Adrenergic receptors mediate stress-induced elevations in extracellular Hsp72

• Published in: Journal of applied physiology (1985) Vol. 99; no. 5; pp. 1789 - 1795
• Main Authors: Johnson, John D, Campisi, Jay, Sharkey, Craig M, Kennedy, Sarah L, Nickerson, Molly, Fleshner, Monika
• Format: Journal Article
• Language: English
• Published: Bethesda, MD Am Physiological Soc 01.11.2005; American Physiological Society
• Subjects: Adrenalectomy; Adrenocorticotropic Hormone - metabolism; Animals; Biological and medical sciences; Catecholamines - metabolism; Electroshock; Extracellular Space - metabolism; Fundamental and applied biological sciences. Psychology; Glucocorticoids - metabolism; HSP72 Heat-Shock Proteins - immunology; HSP72 Heat-Shock Proteins - metabolism; Hypophysectomy; Immune System - physiology; Immunology; Male; Neurotransmitters; Proteins; Rats; Rats, Inbred F344; Receptors, Adrenergic, alpha-1 - metabolism; Signal Transduction - physiology; Stress, Physiological - immunology; Stress, Physiological - metabolism; Tyrosine - pharmacokinetics; circulating; Vertebrata; Mammalia; immune; Rat; Rodentia; Heat shock protein; Norepinephrine; Catecholamine; Adrenergic receptor; Extracellular; Stress
• ISSN: 8750-7587; 1522-1601
• DOI: 10.1152/japplphysiol.00390.2005

Department of Integrative Physiology and Center for Neuroscience, University of Colorado, Boulder, Colorado Submitted 7 April 2005 ; accepted in final form 14 July 2005 Heat-shock protein concentrations in the blood increase after exposure to a variety of stressors, including trauma and psychological stress. Although the physiological function of extracellular heat shock protein remains controversial, there is evidence that extracellular heat shock protein 72 (Hsp72) can facilitate immunologic responses. The signal(s) that mediate(s) the in vivo elevation of extracellular Hsp72 in the blood after stressor exposure remain(s) unknown. Here we report that Hsp72 increases in the circulation via an 1 -adrenergic receptor-mediated signaling pathway. Activation of 1 -adrenoceptors results in a rapid increase in circulating Hsp72, and blockade of 1 -adrenoceptors prevents the stress-induced rise in circulating Hsp72. Furthermore, our studies exclude a role for -adrenoceptors, glucocorticoids, and ACTH in mediating stress-induced elevations in circulating extracellular Hsp72. Understanding the signals involved in elevating extracellular Hsp72 could facilitate the use of extracellular Hsp72 to bolster immunity and perhaps prevent exacerbation of inflammatory diseases during stress. catecholamine; rat; norepinephrine; immune; circulating; heat shock protein Address for reprint requests and other correspondence: J. D. Johnson, Center for Neuroscience, Dept. of Integrative Physiology, Univ. of Colorado at Boulder, Boulder, CO 80309-0354 (e-mail: john.johnson{at}colorado.edu )